Is stressor-evoked cardiovascular reactivity a pathway linking positive and negative emotionality to carotid intima-media thickness?

Stressor-evoked cardiovascular reactivity, trait positive emotionality, and negative emotionality are all associated with cardiovascular disease. It is unknown, however, whether cardiovascular reactivity may constitute a pathway by which trait positive or negative emotionality relates to disease risk. Accordingly, this study modeled the cross-sectional relationships between trait positive and negative emotionality, stressor-evoked cardiovascular reactivity, and severity of a subclinical vascular marker of cardiovascular risk, carotid artery intima-media thickness (CA-IMT). The sample consisted of healthy, midlife adults free from clinical cardiovascular disease (N = 286; ages 30-54; 50% female). Trait positive and negative emotionality were measured by three questionnaires. Heart rate and blood pressure reactivity were assessed across three stressor tasks. CA-IMT was assessed by ultrasonography. Latent factors of positive and negative emotionality, blood pressure reactivity, heart rate reactivity, and CA-IMT were created using structural equation modeling. Greater negative emotionality was marginally associated with more CA-IMT (β = .21; p = .049), but lower blood pressure reactivity (β = -.19; p = .03). However, heightened blood pressure (β = .21; p = .03), but not heart rate reactivity (β = -.05; p = .75), associated with greater CA-IMT. Positive emotionality was uncorrelated with cardiovascular reactivity (blood pressure: β = -.04; p = .61; heart rate: β = .16; p = .11) and CA-IMT (β = .16; p = .07). Although trait negative emotionality associates with a known marker of cardiovascular disease risk, independent of positive emotionality, it is unlikely via a stressor-evoked cardiovascular reactivity pathway.

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Stress-induced blood pressure reactivity and cardiovascular disease risk

The Journal of Physical Fitness and Sports Medicine ◽

10.7600/jpfsm.4.351 ◽

2015 ◽

Vol 4 (5) ◽

pp. 351-356

Author(s):

Ryoko Sone ◽

Nobusuke Tan ◽

Fumio Yamazaki

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Blood Pressure Reactivity ◽

Pressure Reactivity

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Increased vascular α1-adrenergic receptor sensitivity in older adults with posttraumatic stress disorder

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00155.2020 ◽

2020 ◽

Vol 319 (6) ◽

pp. R611-R616

Author(s):

Cortnie L. Hartwig ◽

Justin D. Sprick ◽

Jinhee Jeong ◽

Yingtian Hu ◽

Doree G. Morison ◽

...

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Sympathetic Nerve ◽

Stress Disorder ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Blood Pressure Reactivity ◽

Pressure Reactivity

Posttraumatic stress disorder (PTSD) is an independent risk factor for the development of hypertension and cardiovascular disease. Patients with PTSD have heightened blood pressure and sympathetic nervous system reactivity; however, it is unclear if patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation that could also contribute to increased blood pressure reactivity. Therefore, we hypothesized that patients with PTSD have increased sensitivity of vascular α1-adrenergic receptors (α1ARs), the major mediators of vasoconstriction in response to release of norepinephrine at sympathetic nerve terminals. To assess vascular α1AR sensitivity, we measured the degree of venoconstriction in a dorsal hand vein in response to exponentially increasing doses of the selective α1AR agonist, phenylephrine (PE), in 9 patients with PTSD (age = 59 ± 2 yr) and 10 age-matched controls (age = 60 ± 1 yr). Individual dose-response curves were generated to determine the dose of PE that induces 50% of maximal venoconstriction (i.e., PE ED50) reflective of vascular α1AR sensitivity. In support of our hypothesis, PE ED50 values were lower in PTSD compared with controls (245 ± 54 ng/min vs. 1,995 ± 459 ng/min, P = 0.012), indicating increased vascular α1AR sensitivity in PTSD. The PTSD group also had an increase in slope of rise in venoconstriction, indicative of an altered venoconstrictive reactivity to PE compared with controls (19.8% ± 1.2% vs. 15.1% ± 1.2%, P = 0.009). Heightened vascular α1AR sensitivity in PTSD may contribute to augmented vasoconstriction and blood pressure reactivity to sympathoexcitation and to increased cardiovascular disease risk in this patient population.

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Vitamin D Receptor Activation Mitigates the Impact of Uremia on Endothelial Function in the 5/6 Nephrectomized Rats

International Journal of Endocrinology ◽

10.1155/2010/625852 ◽

2010 ◽

Vol 2010 ◽

pp. 1-10 ◽

Cited By ~ 28

Author(s):

J. Ruth Wu-Wong ◽

William Noonan ◽

Masaki Nakane ◽

Kristin A. Brooks ◽

Jason A. Segreti ◽

...

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Heart Rate ◽

Vitamin D ◽

Endothelial Function ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Receptor Activation ◽

The Impact

Endothelial dysfunction increases cardiovascular disease risk in chronic kidney disease (CKD). This study investigates whether VDR activation affects endothelial function in CKD. The 5/6 nephrectomized (NX) rats with experimental chronic renal insufficiency were treated with or without paricalcitol, a VDR activator. Thoracic aortic rings were precontracted with phenylephrine and then treated with acetylcholine or sodium nitroprusside. Uremia significantly affected aortic relaxation (% in NX rats versus % in SHAM at 30 M acetylcholine). The endothelial-dependent relaxation was improved to –%, –%, and –% in NX rats treated with paricalcitol at 0.021, 0.042, and 0.083 g/kg for two weeks, respectively, while paricalcitol at 0.042 g/kg did not affect blood pressure and heart rate. Parathyroid hormone (PTH) suppression alone did not improve endothelial function since cinacalcet suppressed PTH without affecting endothelial-dependent vasorelaxation. N-omega-nitro-L-arginine methyl ester completely abolished the effect of paricalcitol on improving endothelial function. These results demonstrate that VDR activation improves endothelial function in CKD.

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